TORC1 regulation of dendrite regrowth after pruning is linked to actin and exocytosis.
Journal
PLoS genetics
ISSN: 1553-7404
Titre abrégé: PLoS Genet
Pays: United States
ID NLM: 101239074
Informations de publication
Date de publication:
05 2023
05 2023
Historique:
received:
14
11
2022
accepted:
14
04
2023
revised:
23
05
2023
medline:
25
5
2023
pubmed:
11
5
2023
entrez:
11
5
2023
Statut:
epublish
Résumé
Neurite pruning and regrowth are important mechanisms to adapt neural circuits to distinct developmental stages. Neurite regrowth after pruning often depends on differential regulation of growth signaling pathways, but their precise mechanisms of action during regrowth are unclear. Here, we show that the PI3K/TORC1 pathway is required for dendrite regrowth after pruning in Drosophila peripheral neurons during metamorphosis. TORC1 impinges on translation initiation, and our analysis of 5' untranslated regions (UTRs) of remodeling factor mRNAs linked to actin suggests that TOR selectively stimulates the translation of regrowth over pruning factors. Furthermore, we find that dendrite regrowth also requires the GTPase RalA and the exocyst complex as regulators of polarized secretion, and we provide evidence that this pathway is also regulated by TOR. We propose that TORC1 coordinates dendrite regrowth after pruning by coordinately stimulating the translation of regrowth factors involved in cytoskeletal regulation and secretion.
Identifiants
pubmed: 37167328
doi: 10.1371/journal.pgen.1010526
pii: PGENETICS-D-22-01306
pmc: PMC10204957
doi:
Substances chimiques
Actins
0
Drosophila Proteins
0
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Monomeric GTP-Binding Proteins
EC 3.6.5.2
RalA protein, Drosophila
EC 3.6.5.2
CRTC protein, Drosophila
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1010526Informations de copyright
Copyright: © 2023 Sanal et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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